EC Number   |
General Information |
Reference |
|---|
   2.7.11.16 | malfunction |
depletion of endogenous GRK2 enhances canonical signaling |
705737 |
| 2.7.11.16 | malfunction |
enzyme deficiency contributes to the pathogenesis of Alzheimer's disease by influencing the hyperphosphorylation of tau through the activation of glycogen synthase kinase 3beta |
761592 |
| 2.7.11.16 | malfunction |
enzyme dysfunction is associated with congenital heart defects |
762419 |
| 2.7.11.16 | malfunction |
GRK5 or GRK6 knockdown has no effect on C3aR (G protein coupled receptors for C3a) desensitization, but causes a significant decrease in C3a-induced mast cell degranulation. GRK5 or GRK6 knockdown render mast cells more responsive to C3a for ERK1/2 phosphorylation |
726276 |
| 2.7.11.16 | malfunction |
GRK5-depleted cells are more sensitive to undergoing cell death from polo-like kinase 1 (PLK1) inhibition, and this increased susceptibility corresponds to decreased NPM1 phosphorylation. Conversely, cells with higher GRK5 levels exhibit reduced sensitivity to PLK1 inhibition |
725471 |
| 2.7.11.16 | malfunction |
inhibition of vascular smooth muscle GRK2 enhances beta-adrenergic receptor signaling |
684355 |
| 2.7.11.16 | malfunction |
isoform GRK6 knockdown promotes cell migration and invasion in lung adenocarcinoma cells |
761095 |
| 2.7.11.16 | malfunction |
knockdown of GRK2 or GRK3 expression using shRNA causes a more sustained Ca2+ mobilization, attenuated C3aR (G protein coupled receptors for C3a) desensitization, and enhanced degranulation as well as ERK1/2 phosphorylation when compared to shRNA control cells |
726276 |
| 2.7.11.16 | malfunction |
knockdown of GRK5 expression leads to G2/M arrest, characterized by a prolonged G2 phase, which can be rescued by expression of wild type but not catalytically inactive GRK5 |
725509 |
| 2.7.11.16 | malfunction |
knockdown of GRK5 in osteosarcoma cells inhibits DNAdamage-induced apoptosis via a p53-mediated mechanism |
725394 |
